Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
CNS -1- LOWER LIMB
STEPS OF EXAMINATION
(1) APPROACH THE PATIENT
Read the instructions carefully for clues
Approach the right hand side of the patient, shake hands, introduce yourself
Ask permission to examine him
Expose the lower limbs completely and keep the patient descent (genital area is covered)
(2) GENERAL INSPECTION
STEPS
1. Scan the bedside.
2. Scan the patient.

3. Examine the eyes
4.

Examine the hands: tell the

patient outstretch your hands
like this (dorsum facing
upwards) then like this
(palms facing upwards)
demonstrate. Feel the radial
pulse for AF

POSSIBLE FINDINGS
Walking stick, shoes-callipers, built-up heels
Nutritional status: under/average built or overweight
Abnormal facies: Sad, immobile, unblinking facies
(Parkinsons disease), facial wasting (muscular dystrophy),
facial asymmetry (hemiplegia)
Abnormal movement or posture: rest or intention tremors,
dystonia, choreoathetosis, hemiballismus, myoclonic jerks,
tics, pyramidal posturesee theoretical notes for description,
types, features and causes of abnormal movements
Abnormal facial movements: hemifacial spasm, facial
myokymia, blepharospasm, oro-facial dyskinesia
Scar or deformity underlying an ulnar nerve palsy
Peroneal wasting (Charcot-Marie-Tooth disease)
Pes cavus (Friedreichs ataxia, Charcot-Marie-Tooth disease)
Nystagmus (cerebellar syndrome)
Horners syndrome (syringomyelia, Pancoasts syndrome)
wasted hands (MND, Charcot-Marie-Tooth disease,
syringomyelia)
AF consider thromboembolic complications

(3) INSPECTION OF THE LOWER LIMB

Steps
Possible findings
1. Scan the lower limb.

Muscle bulk: Look specifically for:
2. Note specifically the
 Generalized disuse atrophy (e.g. severe spastic paraparesis)
quadriceps, the anterior
 Unilateral loss of muscle bulk (old polio)
compartment of the shin,
 Distal muscle wasting with preservation of the thigh muscle
the extensor digitorum
bulk (inverted champagne bottle) Charcot-Marie-Tooth
brevis, and the peroneal
disease
muscles.
 Isolated anterior thigh wasting (e.g. diabetic amyotrophy)
3. Compare right with left
 Proximal muscle wasting (polyomyositis)
 Wasting confined to one peroneal region (lateral popliteal =
common peroneal nerve palsy)

Fasciculations: irregular twitches under the skin overlying muscle
at rest; represent contraction of a motor unit. They occur in LMNL;
usually in wasted muscles (nearly always indicate MND). Flicking
the skin over wasted muscle may elicit fasciculations. Nonpathological fasciculations occasionally occurs after vigorous
exercise in healthy people.

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
(4) TONE
1.
2.
3.

4.

Steps
Tell the patient Let your legs go loose and let me move
them for you
Roll the extended leg on the bed, rotating the hip externally
and internally (compare right with left)
Put your hand behind the knee and lift it rapidly (feel for any
catch; watch the heel) and let it drops (compare right with
left)
Hold the knee and ankle. Passively flex and extend the leg at
the knee and hip joints repeatedly in an irregular and
unexpected rhythm (compare right with left)

Possible findings

Normally there is light resistance
through whole range of
movements.

Normally the heel will lift
minimally off the bed when the
knee is lifted quickly

See theoretical notes for
abnormalities of the tone

(5) POWER
Steps
Possible findings
Tell the patient I am going to test the strength of Describe any weakness in terms of the medical
some of your muscles. Fix the joint proximal to research council (MRC) scale from 5 (normal)
the group of muscles you are testing. Give the down to 0 (no visible muscle contraction)see
patient a space to show his power before resisting theoretical notes for the MRC scale for power
him and look at the muscle contracts. Compare grading
right with left
1. Hip flexion: tell the patient keep your leg Action by the iliopsoas (supplied by the femoral
straight and lift it up into the air. Now keep it nerve & direct branches from the lumbar sacral
up and dont let me push it down
plexus; L1,2)
2. Hip extension: tell the patient now push your Action by the glutei (supplied by the inferior gluteal
leg down into the bed and do not let me stop nerve; L4,5)
you
3. Hip abduction: tell the patient push out Action by the glutei (supplied by the superior
against my hands
gluteal nerve; L4,5)
4. Hip adduction: tell the patient push in against Action by the adductor group (supplied by the
my hands
obturator nerve; L2,3,4)
5. Knee flexion: hold the patients ankle and tell Action by the hamstrings (supplied by the sciatic
him (her) bend your knee and pull your heel nerve; L5,S1,2)
towards you; dont let me stop you
6. Knee extension: tell the patient now Action by the quadriceps (supplied by the femoral
straighten your knee out and push my hand
nerve; L3,4)
7. Ankle dorsiflexion: tell the patient pull your Action by the tibialis anterior and long extensors
foot up to you and push my hand
(supplied by the deep peroneal nerve; L4,5)
8. Ankle planter flexion: tell the patient push Action by the gastrocnemius (supplied by the
your foot down against my hand
posterior tibial nerve; S1)
See theoretical notes for:
 Features & causes of the different patterns of weakness
 Clinical approach to weakness
 Motor root values in the lower limb
 Examples of mononeuropathies and radiculopathies in the lower limb

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
(6) REFLEXES
Steps
Explain to the patient. Use a long tendon hammer; flex your
wrist and let the hammer fall with its own weight onto the
muscle. Compare right with left. If the reflex appears to be
absent, ask the patient to clench his teeth as you swing the
hammer (reinforcement).
1. Knee reflex: place the arm under the knee so that the
knee is at 90 degrees. Strike the knee below the patella;
watch the quadriceps
2. Knee (patellar) clonus: with the knee extended, sharply
push the patella downwards with your thumb and
forefinger, sustaining the pressure for a few seconds. Do
not examine for knee clonus (as it is not expected to be
present) if knee reflex is diminished
3. Ankle reflex: hold foot at 90 degrees with a medial
malleolus facing the ceiling. The knee should be flexed
and lying to the side. Strike the Achilles tendon directly.
Watch the muscles of the calf
4. Ankle clonus: support the patients leg with both the
knee and ankle resting in 90 degree flexion. Briskly
dorsiflex and partially evert the foot and sustain the
pressure. Do not examine for ankle clonus (as it is not
expected to be present) if ankle reflex is diminished.
5. Plantar response (Babinskis sign): Explain to the
patient: I am going to scrape the bottom of your foot.
Using a blunt object (orange stick, the end of the reflex
hammer or car key), gently scrape the lateral portion of
the sole beginning near the heel and moving up towards
the little toe then across the foot pad to the base of the
big toe. Watch the big toe and the remainder of the foot.
N.B. Alternative stimuli to elicit the plantar response:

Chaddocks manoeuver: scrape the lateral portion of the
dorsum of the foot beginning near the lateral malleolus
and moving up towards the little toe

Oppenheims sign: with your thumb and index finger,
press heavily from above downwards along the medial
aspect of the tibia

Gordons reflex: pinch the Achilles tendon
6. Abdominal reflexes: the patient should be supine and
relaxed. Using an orange stick lightly scratch the
abdominal wall towards the umbilicus in the four
quadrants of the stomach.

Possible findings
Grade the response from 0 (absent) up to
4+ (clonus) see theoretical notes for
reflexes grading

Reflex arc through the femoral nerve;

L3,4
A rhythmic contraction may be noted. It is
always abnormal and indicates 4+ knee
reflex grading

Reflex arc through the tibial nerve; S1,2

A rhythmic contraction may be noted.

More than three beats is abnormal and
indicates 4+ ankle reflex grading.

Reflex arc through S1,2

always describe the response as either
downgoing, i.e. all the toes flex
towards the plantar surface, or
upgoing where the big toe extends
dorsally (goes up), while the four
small toes fan and turn towards the
sole
See theoretical notes for patterns of
planter response

Normal response is contraction of the

recti with the umbilicus moving away
from the direction of the scratch.

Afferent: segmental sensory nerves

Efferent: segmental motor nerves

Roots: T8,9 above the umbilicus, and
T11,12 below the umbilicus

Abdominal reflexes are absent in
UMNL above their spinal level, and in
LMNL affecting T8-12.

It is often impossible to elicit
abdominal reflexes in anxious patients,
elderly, obese, multiparous women,
and those who have had abdominal
surgery
See theoretical notes for abnormal tendon reflexes, and the root values for reflexes

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin

(7) COORDINATION:
Possible findings
In cerebellar lower limb ataxia, the
patient has difficulty placing or
holding the heel on the opposite knee
or cannot keep the heel firmly on the
tibia as the heel is moved downwards.

Sensory ataxia is similar to cerebellar
ataxia but is markedly worse when the
eyes are closed
2.

Bradykinesia: slowed movements or
break up easily extrapyramidal sign

Dysrhythmia: inability to keep a
rhythm - cerebellar sign
3.

Truncal ataxia is caused by
abnormalities of the midline
cerebellar vermis or the
flocculonodular lobe. It is usually
associated with gait ataxia and
symmetric nystagmus in absence of
limb incoordination
N.B. do not assess coordination if power < 3 (inability to move against gravity), and tell the examiner that
coordination cannot be assessed due to weakness
See theoretical notes for types of ataxia and causes of cerebellar ataxia
1.

Steps
Heel-shin test: the patient is lying supine. Tell the
patient Lift your leg and place the point of your heel on
your knee and then run it down the sharp part of your
shin; now up your shin, now down againetc.
(Demonstrate). Consider repeating the test while the
patients eyes are closed to test for sensory ataxia.
Compare right with left. Expect the right leg to be
slightly better in right handed persons
Rapid repeated movements: Tell the patient tap your
foot quickly on my hand as if listening to fast music
(demonstrate). Compare right with left. Expect the right
leg to be slightly better in right handed persons
Truncal ataxia: ask the patient to sit up with the arms
folded or to rise from a chair with the feet together

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
(8) SENSATION
Steps
Pin prick:

Demonstrate the stimuli to the patient by testing on the sternum
(use each end of the hat pin): explain to the patient this is
sharpand this is bluntnow Im going to test the sensation in
your legs and I want you to close your eyes and say Sharp if it
feels sharp, and blunt if it feels blunt.

Start distally and move proximally testing over each
dermatome (and each main nerve): lateral foot medial foot
outer calf inner calf inner thigh outer thigh inguinal
region. Repeat in the other leg then compare right with left

Map out the boundaries of any area of reduced, absent or
increased sensation; starting from the area of altered sensation
and moving towards normal to find the edges, noting any
difference between the two sides.

If a stocking sensory loss is present, demonstrate that the
sensory loss is present right round the limb.

If compression of the cord is suspected, then demonstrate a
sensory level.
2. Light touch:

Demonstrate I am going to touch you with this piece of cotton
wool and I want you to close your eyes and say (Yes) every time
you feel it. Avoid dragging it across the skin or tickling the
patient. Time the stimuli irregularly to check the patient
reliability.

Start distally and move proximally testing the lower limb in the
same sequence as for pin prick
3. Joint position sense:

Demonstrate: fix the proximal phalanx of the patients big toe
with one of your hands. Hold the lateral aspects of the distal
phalanx of the patients big toe between the thumb and index
finger of your other hand. Ensure that your thumb and index
finger are at 90 degrees to the intended direction of movement.
Tell the patient Im going to move your finger up and down; this
is up (move finger up), and this is down (move finger
down)now close your eyes and tell me whether I am moving
your finger up or down.

Start with the IP joint of big toe. If impaired, move to more
proximal joints progressively (IP MTP ankle knee
hip).
4. Vibration sense:

Demonstrate: use a 128 Hz tuning fork. Make the fork vibrate
and place it on the sternum. Ask the patient Do you feel it
vibrating (buzzing)?

Tell the patient Close your eyes. Make the fork vibrate silently
and place it on the terminal phalanx of the big toe just below
the nail bed and ask the patient Can you feel it now? If patient
cannot feel the vibration, move progressively to more proximal
joints (terminal phalanx of the big toe MTP joint medial
malleolus tibial tuberosity ASIS).
See theoretical notes for:
 Modalities and tracts of sensation
 Patterns, causes and clinical approach to sensory loss
1.

Possible findings
Reduced sensation over
the lateral foot tibial
nerve or S1 lesion
Reduced sensation over
the medial foot
common peroneal nerve
or L5 lesion
Reduced sensation over
the outer calf
common peroneal
nerve or L5 lesion
Reduced sensation over
the inner calf L4
lesion
Reduced sensation over
the inner thigh L3
lesion
Reduced sensation over
the outer thigh lateral
cutaneous nerve of the
thigh or L2 lesion
Reduced sensation over
the inguinal region
L1lesion

N.B. vibration sense is

commonly reduced or absent
in elderly patients

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
(9) GAIT AND ROMBERGS TEST: ask the examiners permission to examine the patients gait and
perform Rombergs test (see Ch 9. CNS Gait).
(10) ADDITIONAL SIGNS: according to diagnosis, e.g.
Look for cataract and scar for pacemaker, palpate for local spinal tenderness and examine for sensory
level
Tell the examiner that you would normally extend your examination to examine the upper limb and
cranial nerves and woud ask about swallowing (Dystrophia myotonica), bladder symptoms, test the
anal tone (spinal cord syndrome), and to dipstick urine for DM.
(11) THANK THE PATIENT AND COVER HIM (HER)

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
THEORETICAL NOTES
HOW TO DESCRIBE AN ABNORMAL MOVEMENT: abnormal movements are described according
to the following fundamental characteristics:
Is the movement present at rest (rest tremors), with holding of a posture (postural tremors), or during a
skilled movement (action or intention tremors)
Is the movement disorder global (generalised dystonia), focal (focal dystonia), unilateral, or confined
to one limb
Is the movement disorder predominantly distal (choreoathetosis) or proximal (hemiballismus) in the
limb
Is the movement sinuous (choreoathetosis), twitchy (myokymia), or shock like (myoclonus)
Does the limb hold abnormal postures for several seconds (dystonia)
TYPES OF ABNORMAL MOVEMENTS
1. Tremors (rest tremor, postural tremor, action tremor, intention tremor)
2. Asterixis
3. Dystonia
4. Chorea
5. Asthetosis
6. Choreoasthetosis
7. Hemiballismus
8. Myoclonic jerks
9. Tics (habit spasms)
10. Dyskinesia
11. Akathisia
TREMORS
Features
Tremors are
oscillatory distal
movements resulting
from alternating
contraction and
relaxation of
muscles. Tremors are
described according
to their speed (fast
or slow), amplitude
(fine or coarse) and
whether they are
maximal at rest, on
maintaining a
posture or on
carrying out an
active movement
(rest, postural,
action or intention)

Types
Causes
Rest tremor: present when limb is 1. Akinetic-rigid syndromes
at rest and reduced by voluntary
(parkinsonism)
movement. It is usually rapid,
rhythmic, alternating tremor,
predominantly in flexion/extension
but often with a prominent rotary
component between finger and
thumb (pill-rolling tremor). It is
almost always more severe in the
arm than in the leg, and is usually
asymmetrical.
Postural tremor: present when
1. Benign essential tremor (50% familial):
limb is maintained in a position
usually coarse tremor and often
against gravity.
exaggerated in awkward postures, as
when the outstretched fingers are held
pointing at each other, in full inversion, in
front of the patients nose.
2. Exaggerated physiological tremor (fine
and rapid): seen with anxiety,
hyperthyroidism, excess alcohol or
caffeine, or -agonists.
Action tremor: present during an 1. Lesions of the red nucleus and subaction
thalamic nucleus (most often caused by
damage from vascular disease or MS)
Intention tremor: most prominent 1. Cerebellar disease
during voluntary movement
towards a target

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
ASTERIXIS
Feature
Asterixis (negative myoclonus): intermittent inhibition of 1.
muscle tone that leads, for example, to a momentary and
repetitive partial flexion of the wrists during attempted
sustained wrist extension (may superficially resemble a 2.
tremor).

Causes
Metabolic encephalopathy (liver
failure, uraemia, poisoning with hypnotic
drugs)
respiratory failure

DYSTONIA
Feature
Dystonia literally means any abnormality of muscle
tone, but most neurologists employ it to describe the
slow development of an abnormal posture (often of
the limb or the neck) which is maintained by cocontraction of both agonists and antagonists.
Positions maintained are usually at an extreme of
extension or flexion. Common forms are torticollis
(the neck twisted to one side), anterocollis (the neck
flexed forward), retrocollis (the neck extended
backwards), lordosis (the arched back), and scoliosis
(twisted back). The arm is usually abducted at the
shoulder, extended at the elbow, pronated to an
extreme position with the fingers extended. The leg
is usually extended at the hip and knee and inverted
at the ankle with the toes flexed. The term dystonia
frequently is qualified as torsion dystonia, to
emphasize the twisted nature of the abnormal
postures

Types
Focal dystonia (affects
only one part of the
body): e.g. isolated
torticollis or isolated
writers

1.
2.
3.

1.
Segmental dystonia
(affecting two or more
adjacent parts of the
body): for example
torticollis and dystonic
posturing in the same arm
1.
Generalised dystonia
(affects parts of the body
that are not adjacent):
2.
often associated with
chorea

CHOREA, ASTHETOSIS, CHOREOASTHETOSIS

Feature
Chorea is a brief, fluid, involuntary movements which
frequently appear pseudo-purposeful. In chorea, the
ordinary voluntary movements, such as walking or
picking up a cup, may be embellished with rapid extra
little flourishes of movement. The outstretched upper
limbs may assume a hyperpronated posture and little
flicks of movement of the digits or wrist, or of the face
and tongue may occur.

1.
2.

3.
4.

Causes
Idiopathic
Major
tranquilisers,
Treated
Parkinsons
disease on
excessive therapy
As for focal
dystonia (see
above)

As for chorea (see

below).
Rare causes:
dystonia
musculorum

Causes
Drug therapy of Parkinsons disease
(excess treatment)
Wilsons disease (look for associated liver
disease and Keyser-Fleischer rings on
cornea)
Huntington's disease (trace family history)
Post-pill or pregnancy chorea (chorea
gravidarum)
Sydenham's chorea
Stroke
The term athetosis was introduced
originally to describe the sinuous, writhing
digital movements that may follow a
stroke. Subsequently, athetosis became
synonymous with one type of cerebral
palsy, resulting from brain damage due to
anoxia or kernicterus at birth.

5.
6.
Athetosis is a complex irregular slow, writhing 1.
movement; occurs nearly continuously in distal muscles.
It consists of an interaction between various postures of
the hand or foot, especially grasping and avoiding. The
fingers are alternately widely extended, the arm
following into an extended, abducted and externally
rotated posture, and then the fingers clench, often
trapping the thumb in the palm, and the limb flexes
slightly and rotates internally.
Choreoathetosis refers to something between the chorea and athetosis (or uncertainty on the part of the
observer!)

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
HEMIBALLISMUS, MYOCLONIC JERKS, TICS, DYSKINESIA, AKATHISIA
Feature
Causes
Hemiballismus (Ballism = to throw) is an irregular 1. Infarction of the contralateral sub-thalamic
sudden and often violent flinging movement of a
nucleus or its connections
proximal limb, usually an arm. It most often involves
only one side of the body (i.e., hemiballism [us]).
There is no clear distinction from sever chorea.
Myoclonic jerks are sudden shock-like contractions 1. Healthy individuals may experience these
of one or more muscles which may be focal or diffuse.
when falling asleep or surprised by a sudden
They may occur singly or repetitively. Myoclonus can
noise
occur spontaneously at rest, in response to sensory 2. Metabolic encephalopathies
stimuli, or with voluntary movements.
3. Myoclonic epilepsies
4. Creutzfeldt-Jakob disease
5. Post-anoxic encephalopathy
Tics (habit spasms) are stereotyped, irresistible 1. Simple tics: isolated transient or chronic tics
movements, which are essentially purposeful
in children that may persist to late adolescence
movements but recurring involuntarily in repetitive
(good prognosis)
manner (may superficially resemble myoclonic jerks 2. Gilles de la Tourette syndrome: tics
but more stereotyped). Tics may be voluntarily
associated with coprolalia (involuntary and
controlled at the expense of mounting inner tension.
inappropriate obscene speech). The
pathophysiology is obscure. A dopaminergic
excess has been suggested by the clinical
observation that the tics may respond to
treatment with dopamine-blocking drugs.
3. Wilson's disease (associated with hepatic and
renal involvement, Kayser-Fleischer corneal
rings, low serum copper and ceruloplasmin
levels, and increased 24-h urinary copper
excretion)
4. Post-encephalitic syndromes
5. Stimulant or neuroleptic medication.
6. In association with obsessive compulsive
disorders.
Dyskinesia literally means any abnormal movement 1. Neuroleptic drugs (dopamine blocking
but the term has become synonymous with drugagents): phenothiazines (chlorpromazine),
induced abnormal movements; particularly orofacial
butyrophenones (haloperidol), substituted
dyskinesia. The term tardive (late) dyskinesia is used
benzamides (metoclopramide), reserpine,
tetrabenazine
to distinguish movement disorders that occur as a late
complication of treatment with neuroleptic drugs from 2. Antiparkinsonian agents (dopamine like
acute dystonia and extrapyramidal syndrome which
effects): L-dopa, bromocriptine, lysuride,
develop early.
pergolide
Akathisia: Motor restlessness where the patient 1. Late reaction to major tranquilisers (tardive
constantly shifts crossing and uncrossing his legs and
akathisia)
walking on spot.

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
ABNORMALITIES OF TONE:
Tone
Features

Slight resistance through whole range of movement.
Normal

Heel will lift minimally off the bed when the knee
is lifted quickly

4.
5.
1.

Causes
Normal
Myopathy normal tone or
hypotonia
Neuromuscular junction
diseases
Functional weakness
LMN Lesion
Cerebellar
Myopathy (normal or
hypotonia)
Spinal shock
Chorea
UMN Lesion

1.

Extrapyramidal syndromes

1.

Bilateral frontal lobe

damage (CVA, dementia)

1.
2.
3.

Hypotonia

Hypertonia




Loss of resistance through movement.

Heel does not lift off the bed when the knee is lifted
quickly.

Spasticity:
 Resistance is velocity-dependent, detected as a
catch at the beginning or end of passive
movement, has a sudden release after reaching a
maximum (the "clasp-knife" phenomenon)
 Heel easily leaves the bed when the knee is lifted
quickly
 Predominantly affects antigravity muscles (upper
limb flexors and lower limb extensors)
Rigidity
 Lead pipe or plastic rigidity: Increased tone
through whole range, as if bending a lead pipe.
 Cogwheel rigidity: Increased tone through whole
range, with regular interruption to the movement
giving it a jerky feel (due to associated tremor)
Paratonia or Gegenhalten:
 Increased tone through whole range that varies
irregularly in response to repetitive passive
movements, becoming worse when the patient
tries to relax (patient apparently opposes your
attempts to move his limb)

4.
1.
2.
3.

THE MEDICAL RESEARCH COUNCIL (MRC) SCALE FOR POWER GRADING:

0 = no muscle contraction visible
1 = flicker of muscle contraction but no movement
2 = movement when gravity eliminated (but not against gravity)
3 = movement against gravity but not against resistance
4- = slight movement against resistance
4 = moderate movement against resistance
4+ = submaximal movement against resistance
5 = normal power (full strength)
N.B. when testing power, allow patient to move the joint through the full range, and look at or feel the
muscle contract

10

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
FEATURES OF THE DIFFERENT PATTERNS OF WEAKNESS
UMN Lesion
LMN Lesion
Muscle
disease
(myopathy)
No wasting
Severe wasting Mild wasting
Muscle bulk
No
Fasciculations No fasciculations Fasciculations
are common
fasciculations
Spasticity
Hypotonia
Normal tone /
Tone
hypotonia
Pyramidal pattern Distal/
Proximal
Pattern of
of weakness
segmental
weakness
weakness
(weak extensors in distribution of
weakness
the arm, weak
flexors in the leg
more distally and
more in the
abductors than
adductors)
Hyperactive
Hypoactive/
hypoactive/
Reflexes
reflexes
absent reflexes
Normal
reflexes
Extensor plantar
Flexor plantar
Flexor plantar
Planter
response
response
response
response

Neuromuscular
junction (NMJ)
disease
No wasting
No
fasciculations
Normal tone /
hypotonia
Fatiguable
weakness

Functional
weakness
No wasting
No
fasciculations
Normal tone
Erratic power

Normal reflexes

Normal
reflexes

Flexor plantar
response

Flexor plantar
response

11

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin
CAUSES OF THE DIFFERENT PATTERNS OF WEAKNESS
1. Spinal cord syndromes; differentiated by sensory signs
UMN

Complete transverse lesion: trauma, spinal cord compression by tumour (usually
Lesion
bony secondaries in vertebra), cervical spondylitis, transverse myelitis, MS,
intraspinal tumours (e.g. meningiomas), spinal abscess, post infectious (usually
viral)

Hemisection of the cord (Brown-Sequard syndrome): Causes as for transection

Central cord: syringomyelia and trauma leading to haematomyelia

Posterior column loss: any cause of complete transection, SCD (vitamin B 12
deficiency), tabes dorsalis

Anterior spinal syndrome: anterior spinal artery emboli or thrombosis.
2. Brainstem lesions: brainstem infarction or haemorrhage(elderly), MS(young patients),
tumours, trauma
3. Hemisphere lesions: infarction, haemorrhage, tumours, trauma, MS
LMN
1. Mononeuropathy:

Compression (Saturday night palsy: compressing radial nerve in spiral groove by
Lesion
leaning arm over chair- also reported to affect sciatic nerve after falling asleep
sitting on toilet)

Entrapment, e.g. median nerve in carpal tunnel, common peroneal nerve behind
head of the fibula at the knee; more common in DM, RA, hypothyroidism and
acromegaly
2. Radiculopathy:

Cervical or lumbar disc protrusion, e.g. L5/S1 disc protrusion compresses the S1
root.

At the level of a compressive spinal lesion (secondary tumours, neurofibroma)
3. Peripheral neuropathies:

Acute predominantly motor neuropathies: Guillan-Barre syndrome, diphtheria,
porphyria

Subacute sensorimotor neuropathy: vitamin B1, B12 deficiencies, heavy metal
poisoning (lead, arsenic, thallium), drugs (vincristine, isoniazid), uraemia

Chronic sensorimotor neuropathy: either acquired (DM, hypothyroidism,
paraproteinaemia, amyloidosis) or inherited (HSMN, e.g. Charcot-Marie-Tooth
disease)
4. Mononeuritis multiplex: inflammatory (PAN, RA, SLE, sarcoidosis)
5. Polyradiculopathy: indicates lesion of many roots. It is distinct from other peripheral
neuropathies because it produces a more proximal weakness. The term is commonly
applied to Guillan-Barre syndrome
1. Inherited: muscular dystrophies (Duchenes, Beckers, fascio-scapular-humeral,
Muscle
myotonic dystrophy)
disease
(myopathy) 2. Inflammatory: polyomyositis, dermatomyositis, PMR
3. Endocrine: steroid-induced, hyperthyroid, hypothyroid
4. Metabolic (rare): glycogen storage disease (e.g. Pompes disease), McArdles disease
5. Toxic: alcohol, chloroquine, clofibrate
1. myasthenia gravis: usually idiopathic; occasionally drug-induced (penicillamine,
NMJ
hydralazine)
2. Lambert-Eaton syndrome: paraneoplastic syndrome (usually oat cell carcinoma)
Functional 1. may indicate hysterical illness
weakness

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CLINICAL APPROACH TO WEAKNESS

Features of weakness
Possible diagnosis
Generalized weakness
1. Diffuse disease of nerve: poly-radiculopathy
(limbs and cranial nerves)
2. Diffuse disease of muscle: myopathy
3. Diffuse disease of NMJ: myasthenia gravis
Quadriparesis with
1. Cervical cord lesion
exaggerated reflexes and
2. Brainstem lesion
extensor plantar response
3. Bilateral cerebral lesions.
(i.e. UMN lesion pattern)
Discriminate by sensory testing, cranial nerve signs, and hemisphere signs
Quadriparesis with
1. Poly-radiculopathy
hypoactive/absent reflexes
2. Peripheral neuropathy
(i.e. LMN lesion pattern)
3. Myopathy (normal/hypoactive reflexes): proximal weakness and normal sensations
4. Acute UMNL in the state of spinal shock
Quadriparesis with mixed
1. MND (normal sensations)
UMNL pattern (in the legs)
2. Combined cervical myelopathy and radiculopathy (with sensory loss)
& LMNL pattern (in the
arms)
Quadriparesis with
1. Myopathy: (normal/hypoactive reflexes): proximal weakness and normal
sensations
normal reflexes
2. Myasthenia gravis: fatigable weakness with associated cranial nerve abnormalities
Hemiparesis (UMNL
1. Hemisection of cervical cord
pattern with contralateral
sensory findings
Hemiparesis (UMNL
1. Brainstem lesion
pattern with contralateral

III nerve palsy midbrain lesion
cranial nerve lesion

VI and/or VII pontine lesion

XII IX and XI medullary lesion
Hemiparesis (UMNL
1. Internal capsule lesion
pattern with ipsilateral
UMNL VII palsy
Hemiparesis (UMNL
2. Cerebral lesion
pattern with hemisphere

Parietal lobe lesion contralateral lower homonymous quadrantanopia
signs (aphasia, higher

Temporal lobe contralateral upper homonymous quadrantanopia
function deficits,

Lesion in the anterior occipital cortex (posterior cerebral artery occlusion)
contralateral visual field
congruous homonymous hemianopia
defects, contralateral

Bilateral occipital lobe lesions cortical blindness
inattention or neglect)
Paraparesis (UMNL
pattern)
Paraparesis (LMNL
pattern)

Monoparesis (UMNL
pattern)

Monoparesis (LMNL
pattern)
Patchy weakness (UMNL
pattern)
Patchy weakness (LMNL
pattern)
Variable weakness (non
anatomical distribution)

1.

Spinal cord lesion above the root level of the highest motor abnormality. A level
may be ascertained with sensory signs (sphincter involvement)
1. Polyradiculopathy
2. Cauda equinal lesion (sphincter involvement)
3. Peripheral neuropathy:

Acute (Guillan-Barre syndrome, porphyria, diphtheria)

Subacute (lead poisoning)

Chronic (HSMN, CIDP)
1. Lesion in spinal cord (above the highest involved level)
2. Brainstem lesion
3. Cerebral lesion.
Discriminate by sensory testing, cranial nerve signs, and hemisphere signs.
1. Mononeuropathy
2. Radiculopathy
See examples of mononeuropathies and radiculopathies below
1. Multiple CNS lesions
1.
2.
1.
2.

Polyradiculopathy
Multiple single nerves (mononeuritis multiplex)
If progressively gets worse: consider myasthenia gravis
If fluctuates; giving full power at times: consider functional weakness

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MOTOR ROOT VALUES IN THE LOWER LIMB
Root value
Muscle action
L1,2,3
Hip flexion
L2,3
Hip adduction
L4,5,S1
Hip abduction
L5,S1
Hip extension
L3,4
Knee extension
L4,5
Ankle dorsiflexion and inversion
L5,S1
Ankle eversion
S1,2
Ankle plantar flexion
L5,S1,2
Knee flexion
L5,S1
Toes extension
S2,3
Toes flexion
EXAMPLES OF MONONEUROPATHIES AND RADICULOPATHIES IN THE LOWER LIMB
Common peroneal palsy
L4 root
L5 root
S1 root
(compare to L5)
Foot drop high stepping gait
Weakness of
Weakness of foot
Weakness of
dorsiflexion, inversion
plantar flexion
knee extension
Wasting of the muscles on the
and foot eversion
and foot
and eversion, extension
lateral aspect of the leg (tibialis
of the big toe and hip
dorsiflexion
anterior and peronei)
Loss of ankle
abduction
reflex
Loss of knee
Weakness of dorsiflexion

Sensory loss over the

reflex
(tibialis anterior; L5) and
Sensory loss over
lateral shin and dorsum
the lateral border
eversion (peronei; S1).
Sensory loss
of
foot
of foot and sole
over
the
medial
Sensory loss over the
of foot
shin
anterolateral aspect of the lower
half of the leg (lateral shin) and
dorsum of the foot
Characteristically: ankle reflex is
preserved (lost in tibial nerve
palsy, sciatic nerve palsy and S1
radiculopathy)
Ankle inversion is intact (lost in
tibial nerve palsy, sciatic nerve
palsy and L4/5 radiculopathy)
CAUSES OF FOOT DROP
1. Common peroneal nerve palsy (ankle eversion is lost while ankle inversion and ankle reflex are
preserved)
2. Lumbosacral plexus lesion
3. Sciatic nerve palsy (ankle reflex and ankle inversion are lost)
4. Peripheral neuropathy, especially HSMN type 1
5. L4/5 radiculopathy most commonly due to prolapsed lumbar disc (ankle reflex and ankle inversion are
lost)
6. Motor neurone disease (MND)

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REFLEXES GRADING
0 = absent
= present only with reinforcement
1+ = present but depressed (diminished)
2+ = normal
3+ = increased (hyperactive)
4+ = clonus
ABNORMAL TENDON REFLEXES
Reflex response
1.
Increased reflex or clonus
1.
Absent reflexes
2.
3.

Reduced reflexes
Inverted reflex: a combination
of loss of the reflex tested with
spread of the reflex to muscle at a
lower level. It is caused by
combined spinal cord and root
lesion

Pendular reflex
Slow relaxing (myotonic) reflex

Causes
UMNL above the level of the increased reflex
Generalized peripheral neuropathy
Isolated root lesion or less commonly peripheral nerve lesion
Bilateral absent ankle reflexes peripheral neuropathy or -less
commonly- bilateral S1 root lesions or -very rarely- bilateral
sciatic nerve lesions
N.B. reflexes can be absent in the early stages of severe UMNL (spinal
shock)
1. Peripheral neuropathy, muscle disease and cerebellar syndrome.
1. The level of the absent reflex indicates the level of the lesion. For
example, in an inverted biceps reflex, when the biceps tendon is
tapped there may be no biceps reflex but the triceps contracts; this
indicates LMNL at the level of the absent reflex (in this case C5)
with UMNL below; indicating spinal cord involvement at the
level of the absent reflex. In an inverted supinator reflex, when the
supinator reflex is tested there is no response but finger flexion
occurs (C5/6 lesion)
1. Best seen in the knee jerk where the reflex continues to swing for
several beats. This is associated with cerebellar disease
1. Especially seen at the ankle reflex and may be difficult to note. It
is associated with hypothyroidism.

THE ROOT VALUES FOR REFLEXES

Action
One two....buckle my shoe
Three four... .kick the door
Five six.pick up sticks
Seven eight ..shut the gate

Root values
S 1,2
L 3,4
C5
C6
C7
C8

PATTERNS OF PLANTAR RESPONSE

Response
Flexor plantar response (negative Babinskis sign): all the toes
flex towards the plantar surface
Extensor plantar response (positive Babinskis sign): The big
toe extends dorsally (goes up), while the four small toes fan and
turn towards the sole.
Withdrawal response: The big toe extends (goes up), the other
toes extend and ankle dorsiflexes
No response: no movement of the big toe (even if the other toes
flex)

Reflexes
Ankle reflex
Knee reflex
Biceps reflex
Brachioradialis reflex
Triceps reflex
Finger reflex








What it means
Normal
UMNL above the S1 level of the
spinal cord
Normal in children below the age
of 1 year
Repeat more gently or try
alternative stimuli
profound UMN weakness (toe
unable to extend)
Sensory abnormality interfering
with the afferent part of the reflex.

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TYPES AND CAUSES OF ATAXIA

Features
Cerebellar Abnormalities of the
limb ataxia intermediate and lateral
portions of the
cerebellum typically
produce impaired limb
movements rather than
truncal ataxia. If
involvement is
asymmetric, lateralized
imbalance is common
and usually associated
with asymmetric
nystagmus

Cerebellar
truncal
ataxia

Sensory
limb ataxia

Abnormalities of the
midline cerebellar vermis
or the flocculonodular
lobe produce truncal
ataxia which is usually
revealed during the
process of rising from a
chair, assuming the
upright stance with the
feet together, or
performing some other
activity while standing.
Porprioceptive
impairment produced
sensory limb ataxia,
which is similar to
cerebellar limb ataxia but
is markedly worse when
the eyes are closed.
Examination also reveals
abnormal proprioception
and vibratory perception.

Causes
Unilateral limb ataxia
(ipsilateral cerebellar
syndrome):
 Demyelination,
 Vascular disease
 Less commonly trauma,
tumour or abscess
Bilateral limb ataxia
(bilateral cerebellar
syndrome):
 Drugs; e.g.
anticonvulsants
(phenytoin)
 Alcohol
 Demyelination (MS)
 Vascular disease (stroke)
 Less commonly
hereditary cerebellar
degeneration
(Friedreichs ataxia),
paraneoplastic disorders,
or hypothyroidism
Lesion of the cerebellar
vermis (Midline cerebellar
syndrome): cause as for
bilateral cerebellar syndrome

Porprioceptive impairment:
 Peripheral nerves lesions
 Posterior column lesion
 Parietal lobe damage

MODALITIES AND TRACTS OF SENSATION

Vibration and joint position
Pin prick and temperature
Ascend in the posterior column Ascend in the spinothalamic tract
(remains ipsilateral up to the (crosses within one to two
medulla, where it crosses over)
segments of entry)

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Associated clinical signs

Dysmetria and intention
tremor (finger-nose and
heel-shin tests)
 Dysdiadochokinesia
(rapid alternating
movements)
 Muscle tone is often
modestly reduced; this
contributes to the
abnormal rebound due to
decreased activation of
segmental spinal cord
reflexes and also to
pendular reflexes, i.e., a
tendency for a tendon
reflex to produce
multiple swings to and
fro after a single tap


Gait ataxia and

symmetric nystagmus in
absence of limb
incoordination

Depends on the site of the

proprioceptive impairment:
 The peripheral nerves
depressed or absent
reflexes
 The posterior columns of
the spinal cord
spasticity with extensor
plantar response
 The parietal lobe (rare)
lateralized imbalance

Light touch
Ascends in both the posterior
column and spinothalamic tracts.

Pearls in PACES- CNS (Lower Limb)

Adel Hasanin

PATTERNS AND CAUSES OF SENSORY LOSS

Sensory lesion
Pattern
Single nerve lesion most commonly
Mononeuropathy
median, ulnar, peroneal, lateral cutaneous
nerve to the thigh

Mononeuritis
multiplex

Multiple single nerve lesions

Radiculopathy

Root or roots lesions most commonly C5,

C6 and C7, L4, L5 and S1
Peripheral nerves lesions: sensory loss
either in both legs or in both arms and legs without clear upper level distal glove
and stocking deficit

Peripheral
neuropathy

Spinal cord lesion

sensory loss in both
legs (or both arms and
both legs) with clear
upper level.

Complete transverse lesion

hyperaesthesia at the upper level with loss
of all modalities a few segments below the
lesion.
Hemisection of the cord (Brown-Sequard
syndrome) loss of joint position sense
and vibration sense on the same side as the
lesion and pain and temperature on the
opposite side a few levels below the lesion.

Brainstem lesion

Thalamic sensory loss

Cortical loss

Functional loss

Causes
Entrapment neuropathy (e.g. median
nerve in carpal tunnel, common peroneal
nerve behind head of the fibula at the
knee, more common in DM, rheumatoid
arthritis, hypothyroidism)

May be presentation of more diffuse
neuropathy (see cause of peripheral
neuropathy below)
DM, connective tissue disease (SLE, RA),
vasculitis (PAN, Churg-Strauss), infection
(HIV), malignancy, or may be presentation of
more diffuse neuropathy (see above)
Compression by prolapsed intervertebral
discs, tumours (e.g. neurofibromatosis)
DM, Vitamin B1, B12 deficiencies, Uraemic
neuropathy, Alcohol, Drugs (vincristine,
isoniazid), Carcinomatous neuropathy
(especially CA bronchus), Amyloidosis, and
Leprosy
Trauma, spinal cord compression by tumour
(usually bony secondaries in vertebra),
cervical spondylitis, transverse myelitis, MS,
intraspinal tumours (e.g. meningiomas),
spinal abscess, post infectious (usually viral)
As for transection

Central cord lesion loss of pain and

temperature sensation at the level of the
lesion, where the spinothalamic fibres cross
in the cord, with other modalities preserved
(dissociated sensory loss).
Posterior column lesion loss of joint
position sense and vibration sense with
intact pain and temperature.

Syringomyelia and trauma leading to

haematomyelia

Anterior spinal syndrome loss of pain

and temperature below the level with
preserved joint position sense and vibration
sense.
Hemisensory loss including face on the
contralateral side): loss of pain and
temperature on the face and on the opposite
side of the body
Hemisensory loss of all modalities
including face on the same side)
Hemisensory loss including face on the
same side): parietal lobe- the patient is able
to recognize all sensations but localizes
them poorly- loss of two point
discrimination, astereognosis, sensory
inattention
This is suggested by a non-anatomical
distribution of sensory deficit frequently
with inconstant findings

Anterior spinal artery emboli or thrombosis

Any cause of complete transection, SCD

(vitamin B 12 deficiency), tabes dorsalis

Demyelination (young patients), brain stem

stroke (lateral medullary syndrome), brain
stem tumours
Stroke, cerebral tumour, MS, trauma
As for thalamic sensory loss

May indicate hysterical illness; however, this

is a difficult diagnosis to make in the absence
of appropriated psychopathology

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CLINICAL APPROACH TO SENSORY LOSS

Features of sensory loss
Sensory loss in the distribution of a single nerve
Sensory loss in the distribution of a single root
Sensory loss affecting both legs with clear upper
level
Sensory loss affecting both legs (or both arms and
both legs) without clear upper level (glove and
stocking)
Sensory loss affecting both arms and both legs
with clear upper level
Hemisensory loss including the face on the same
side (all modalities)
Hemisensory loss including the face on the same
side (not all modalities)
Hemisensory loss including the face on the
contralateral side

Possible diagnosis
Mononeuropathy; most commonly median, ulnar,
peroneal, or lateral cutaneous nerve to the thigh
Radiculopathy; most commonly (C5, C6, C7) or
(L4, L5 and S1)
Spinal cord lesion
Peripheral neuropathy

Cervical spinal cord lesion

Thalamic lesion
Internal capsule lesion
Brain stem lesion

SCIATIC NERVE (L4,5,S1,2,3): most important branch of lumbosacral plexus and largest nerve in the
body. It terminates by dividing into medial popliteal (tibial) and lateral popliteal (common peroneal)
nerves
LATERAL POPLITEAL (COMMON PERONEAL) NERVE (L4,5,S1,2):
Passes through the popliteal fossa, winding around the head of the fibula (more susceptible to injury
than the tibial nerve)
Divides into terminal pressures: deep peroneal (anterior tibial) and superficial nerves
Common peroneal nerve palsy (CPNP):
 Foot drop high stepping gait
 Wasting of the muscles on the lateral aspect of the leg (tibialis anterior and peronei)
 Weakness of dorsiflexion (tibialis anterior; L5) and eversion (peronei; S1).
 Sensory loss over the anterolateral aspect of the lower half of the leg and dorsum of the foot
 Characteristically: ankle reflex is preserved (lost in tibial nerve palsy, sciatic nerve palsy and S1
radiculopathy)
 Ankle inversion is intact (lost in tibial nerve palsy, sciatic nerve palsy and L4/5 radiculopathy)

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